Rhinitis-induced anosmia leads to the disappearance of olfactory-triggered migraine attacks

Dear Editor,

Many conditions have been shown to provoke migraines and most patients have one or more typical precipitating factors. Odours are one of the trigger factors known to provoke migraines with relative ease and frequency (1). Osmophobia is more common in patients with migraine than in other headache disorders, and its presence can help distinguish migraine from other primary headaches (2).

Previous studies have suggested that the relationship between odour and migraine involves the peripheral trigemino-nociceptive system or neuronal hyperexcitability of central trigeminal structures (1). However, the exact mechanism through which odour precipitates migraine attacks and the importance of this mechanism are unclear.

We report a 52-year-old woman suffering from migraines triggered by noxious odours, who became migraine-free after she lost her olfactory function following an episode of severe rhinitis. The patient has suffered from headaches since her twenties. Her typical headaches were a seven out of 10 in severity, pulsating in nature, involved her right temporal area and were associated with nausea. Most attacks were triggered by chemical odours including car exhaust, perfumes and tobacco smoke, among others. Her migraines typically lasted for 24– 36 hours and occurred two to three times per month.

Four months before her visit to our neurology clinic, the patient had an upper respiratory infection (URI) with runny nose and coughing. After recovery from the URI, she reported that she could not smell anything. Three months later, her anosmia had not improved. She underwent rhinoscopic examination that revealed atrophic mucosae in the nasal cavity; the patient scored zero points in smell detection and identification tests. Her neurological examination and the brain magnetic resonance imaging were normal.

Surprisingly, after the patient became anosmic, the migraines ceased. Initially, she was treated for anosmia only with a nasal steroid spray. After 2 weeks of nasal spray treatment, the patient reported no improvement. The patient received stellate ganglion blocks 12 times, which are known to be effective in treating anosmia. However, her sense of smell did not recover, the results of follow-up tests did not vary from baseline and she did not experience any migraines for the following 12 months.

This case illustrates how odour can be an important migraine trigger factor. The injury of olfactory nerve terminals along with atrophy of the nasal mucosa can reduce or prevent migraine attacks. This case adds to clinical examples explaining the pathophysiology of olfactory-induced migraine attacks via transient receptor potential ankyrin 1 (TRPA1) pathways (1). Irritants into the nasal mucosa can produce meningeal vasodilatation by a TRPA1- and Calcitonin gene-related peptide (CGRP) -dependent mechanism.

It is possible that the disappearance of migraine was unrelated to anosmia; thus, other factors cannot be ruled out as the cause of this condition. In particular, the possibility that anosmia-treatment regimens could influence migraine frequencies should also be considered (3).

In summary, we experienced a patient with migraine apparently triggered by odours who became migraine-free after she lost her olfactory function. We hypothesize that sensory factors can be important triggers in migraines, as were proven experimentally.